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Article Abstract

A growing body of behavioral and molecular genetics literature has indicated that the development
of attention-deficit/hyperactivity disorder (ADHD) may be attributed to both genetic and environmental
factors. Family, twin, and adoption studies provide compelling evidence that genes play a strong
role in mediating susceptibility to ADHD. Molecular genetic studies suggest that the genetic architecture
of ADHD is complex, while the handful of genome-wide scans conducted thus far is not conclusive.
In contrast, the many candidate gene studies of ADHD have produced substantial evidence implicating
several genes in the etiology of the disorder. For the 8 genes for which the same variant has
been studied in 3 or more case-control or family-based studies, 7 show statistically significant evidence
of association with ADHD based on pooled odds ratios across studies: the dopamine D4 receptor
gene (DRD4), the dopamine D5 receptor gene (DRD5), the dopamine transporter gene (DAT), the
dopamine β-hydroxylase gene (DBH), the serotonin transporter gene (5-HTT), the serotonin receptor
1B gene (HTR1B), and the synaptosomal-associated protein 25 gene (SNAP25). Recent pharmacogenetic
studies have correlated treatment nonresponse with particular gene markers, while preclinical
studies have increased our understanding of gene expression paradigms and potential analogs for human
trials. This literature review discusses the relevance and implications of genetic associations with
ADHD for clinical practice and future research.